FKRP-dependent glycosylation of fibronectin regulates muscle pathology in muscular dystrophy.

In line with this premise, subjecting larval zebrafish to a newly developed passive force assay 22 revealed that fkrp −/− mutants exhibited a severe and highly significant reduction in their ability to transmit passive force (Fig. 2g ), a reduction not evident in either dag1 − / − mutants nor wild-type sibling controls (Fig. 2g ).

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